The Wolff–Parkinson–White syndrome (WPW) is a ventricular preexcitation syndrome involving the electrocardiographic combination of bundle branch block and shortened PR interval; a number of these patients, who are healthy with otherwise normal hearts, experience recurrent episodes of supraventricular tachycardias (Box 20.1). The basic issue responsible for these clinical findings is the accessory pathway, an abnormal electrical connection that bypasses the atrioventricular (AV) node and creates a direct electrical connection between the atria and ventricles. Electrical impulses within the atria bypass the AV node and His‐Purkinje system using this accessory pathway, activating the ventricular myocardium both directly and earlier than expected. The resultant ventricular depolarization is due to a combination of impulses traveling through both the AV node and the accessory pathway. Aside from establishing the abnormal electrical connection between the atria and the ventricles, the accessory pathway also provides uncontrolled conduction; this “uncontrolled conduction” means that any and all electrical impulses that arrive at the accessory pathway will be transmitted to the ventricle without delay. This “uncontrolled conduction” produces the risk of extremely rapid ventricular rates and the loss of protection by the AV node (which limits the number of impulses that travel to the ventricle via the AV node).

When in sinus rhythm, the classic electrocardiographic triad of WPW includes the following features (Figure 20.1):

1. PR interval less than 0.12 seconds;
   
2. Initial slurring of the QRS complex, known as a delta wave; and
   
3. Widened QRS complex with a duration greater than 0.12 seconds.

The PR interval is shortened because the impulse progressing down the accessory pathway is not subjected to the physiological slowing that occurs in the AV node (Figure 20.1). Thus, the ventricular myocardium is activated by two separate pathways, resulting in a fused, or widened, QRS complex. The initial part of the QRS complex, the delta wave, represents aberrant activation through the accessory pathway; the terminal portion of the QRS complex represents activation of the remaining ventricular myocardium, via both the accessory pathway and the His‐Purkinje system (Figure 20.1).

To be diagnosed with the WPW syndrome, the patient must demonstrate the electrocardiographic findings in sinus rhythm noted above as well as symptomatic tachydysrhythmias, including paroxysmal supraventricular tachycardia (PSVT, including both the NCT and wide complex tachycardia [WCT] varieties) (70%), atrial fibrillation (25%), atrial flutter (5%), and ventricular fibrillation (rare). The most common tachycardia in WPW is PSVT; from an electrophysiologic perspective, this form of tachycardia is termed an atrioventricular reentrant tachycardia. WPW PSVT can present in one of two types as separated by and identified via the width of the QRS complex: narrow and wide QRS complex tachycardias. Narrow complex tachycardia (NCT), the most common dysrhythmia of symptomatic WPW, is characterized by the following conduction features: forward electrical conduction from the atria to the ventricle through the AV node and retrograde movement of the impulse via the accessory pathway from the ventricle to the atria (Figure 20.2a). The QRS complex is narrow because of the depolarization wave’s use of the ventricular conduction pathway, producing rapid, efficient movement of the impulse throughout the ventricles. This conduction loop, if sustained, will produce a rapid, regular, narrow QRS complex tachycardia (Figure 20.2a).